Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.
Alteration of pulmonary immunity to Listeria monocytogenes by diesel exhaust particles (DEPs). I. Effects of DEPs on early pulmonary responses.
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DOI：
10.1289/ehp.021101105
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发表时间：
2002-11
影响因子：
10.4
通讯作者：
Ma JK
中科院分区：
文献类型：
--
作者：
Yin XJ;Schafer R;Ma JY;Antonini JM;Weissman DD;Siegel PD;Barger MW;Roberts JR;Ma JK
据推测，柴油机尾气颗粒（DEP）会通过先天免疫机制和细胞介导的免疫机制加重肺部细菌感染。为了检验这一假设，我们使用大鼠单核细胞增生李斯特菌感染模型研究了 DEP 暴露对肺泡巨噬细胞 (AM) 和肺引流淋巴结淋巴细胞功能的影响。在本研究中，我们重点关注 DEP 暴露对 AM 功能的影响，包括吞噬细胞活性和促炎细胞因子的分泌。李斯特菌感染模型的特征是感染后 3 天和 7 天支气管肺泡灌洗 (BAL) 液中中性粒细胞计数、白蛋白含量和无细胞乳酸脱氢酶活性增加。短期吸入 DEP（50 和 100 mg/m(3)，4 小时）可导致李斯特菌肺部清除率出现剂量依赖性抑制，细菌计数最高出现在第 3 天。这种加重的细菌感染与 DEP 对巨噬细胞功能的抑制作用一致。 DEP 以剂量依赖性方式抑制 AM 的吞噬作用以及李斯特菌诱导的白细胞介素 1ss (IL-1ss) 和 IL-12 的基础分泌。 BAL 液中 IL-1ss 和 IL-12 的量也因 DEP 暴露而减少。此外，DEP 还能减少李斯特菌诱导的脂多糖刺激的 AM 分泌肿瘤坏死因子-α (TNF-α)、IL-1ss 和 IL-12。这些结果表明，DEP 通过抑制 AM 吞噬作用来延缓细菌清除，并通过抑制 AM 分泌 IL-1ss 和 TNF-α 来削弱先天免疫。 DEP 还可以通过抑制 AM 分泌 IL-12 来抑制细胞介导的免疫，IL-12 是李斯特菌感染中启动 1 型辅助 T 细胞发育的关键细胞因子。
It has been hypothesized that diesel exhaust particles (DEPs) aggravate pulmonary bacterial infection by both innate and cell-mediated immune mechanisms. To test this hypothesis, we investigated the effects of DEP exposure on the functions of alveolar macrophages (AMs) and lymphocytes from lung-draining lymph nodes using a rat Listeria monocytogenes infection model. In the present study, we focused on the effects of DEP exposure on AM functions, including phagocytic activity and secretion of proinflammatory cytokines. The Listeria infection model was characterized by an increase in neutrophil count, albumin content, and acellular lactate dehydrogenase activity in the bronchoalveolar lavage (BAL) fluid at 3 and 7 days postinfection. Short-term DEP inhalation (50 and 100 mg/m(3), 4 hr) resulted in a dose-dependent suppression of lung clearance of Listeria, with the highest bacteria count occurring at day 3. This aggravated bacterial infection was consistent with the inhibitory effect of DEPs on macrophage functions. DEPs suppressed phagocytosis and Listeria-induced basal secretion of interleukin-1ss (IL-1ss) and IL-12 by AMs in a dose-dependent manner. The amount of IL-1ss and IL-12 in the BAL fluid was also reduced by DEP exposure. In addition, DEPs decreased Listeria-induced lipopolysaccharide-stimulated secretion of tumor necrosis factor-alpha (TNF-alpha), IL-1ss, and IL-12 from AMs. These results suggest that DEPs retard bacterial clearance by inhibiting AM phagocytosis and weaken the innate immunity by inhibiting AM secretion of IL-1ss and TNF-alpha. DEPs may also suppress cell-mediated immunity by inhibiting AM secretion of IL-12, a key cytokine for the initiation of T helper type 1 cell development in Listeria infection.
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影响因子：
56.9
作者：
Fearon, DT;Locksley, RM
通讯作者：
Locksley, RM
影响因子：
10.4
作者：
JAKAB, GJ;RISBY, TH;FARRINGTON, JE
通讯作者：
FARRINGTON, JE
影响因子：
3.8
作者：
JAKAB, GJ
通讯作者：
JAKAB, GJ
影响因子：
4.5
作者：
BOND, JA;MAUDERLY, JL;WOLFF, RK
通讯作者：
WOLFF, RK
影响因子：
4.5
作者：
Fujimaki, H;Saneyoshi, K;Endo, T
通讯作者：
Endo, T